The study, funded by the British Heart Foundation and published in the journal Nutrition and Diabetes, found the sugar substance destabilised High Density Lipoprotein (HDL) cholesterol, a so called ‘good’ cholesterol that helped remove excess levels of bad cholesterol from the body, in people with type-2 diabetes.
The HDL cholesterol damaged by methylglyoxal (MG) was quickly cleared from the blood or else stayed in the plasma without its beneficial heart function.
Lead researcher Dr Naila Rabbani said MG damage was a “new and likely important” cause of low and dysfunctional HDL, and could constitute to a 9% risk of heart disease. Increased levels of MG was common in the elderly and those with diabetes or kidney problems.
Change through diet
The main source of MG was the body, produced as a by-product when glucose was metabolised, but it can also come from the diet, particularly processed foods high in sugar. Dr Rabbani told FoodNavigator her team had looked at boosting the protective protein enzyme glyoxalase 1 (Glo 1) in the blood through diet to counter this effect, something she said was favourable to reducing sugar intakes since MG required a “very reactive” solution.
"This means that in future we have both new drugs and new foods that can help prevent and correct low HDL, all through the control of MG,” she said.
The research sought to characterise the extent of HDL modification by methylglyoxal and the functional consequences in 22 otherwise healthy type 2 diabetes sufferers, a group with a high risk of cardiovascular disease. The average age of the subjects was 38 years.
Rabbani and her colleagues also created a mathematical model that calculated the the risk of cardiovascular disease in an ageing population was increased two fold, while this was three fold for those with diabetes and four to five fold for those with renal failure.
Source: Nutrition & Diabetes
Published online ahead of print, doi:10.1038/nutd.2014.31
“Arginine-directed glycation and decreased HDL plasma concentration and functionality”
Authors: L. Godfrey, N. Yamada-Fowler, J. Smith, P.J. Thornalley and N. Rabbani